The combined effects of temperature and posture on regional blood flow and haemodynamics.

Under simultaneous ambient temperature and postural stressors, integrated regional blood flow responses are required to maintain blood pressure and thermoregulatory homeostasis. The aim of the present study was to assess the effect of ambient temperature and body posture on regional regulation of microvascular blood flow, specifically in the arms and legs. Participants (N = 11) attended two sessions in which they experienced transient ambient conditions, in a climatic chamber. During each 60-min trial, ambient temperature increased from 15.7 (0.6) °C to 38.9 (0.6) °C followed by a linear decrease, and the participants were either standing or in a supine position throughout the trial; relative humidity in the chamber was maintained at 25.9 (6.6) %. Laser doppler flowmetry of the forearm (SkBFarm) and calf (SkBFcalf), and haemodynamic responses (heart rate, HR; stroke volume, SV; cardiac output, CO; blood pressure, BP), were measured continuously. Analyses of heart rate variability and wavelet transform were also conducted. SkBFarm increased significantly at higher ambient temperatures (p = 0.003), but not SkBFcalf. The standing posture caused lower overall SkBF in both regions throughout the protocol, regardless of temperature (p < 0.001). HR and BP were significantly elevated, and SV significantly lowered, in response to separate and combined effects of higher ambient temperatures and a standing position (all p < 0.05); CO remained unchanged. Mechanistic analyses identified greater sympathetic nerve activation, and higher calf myogenic activation at peak temperatures, in the standing condition. Mechanistically and functionally, arm vasculature responds to modulation from both thermoregulation and baroreceptor activity. The legs, meanwhile, are more sensitive to baroreflex regulatory mechanisms.

A sensorimotor enhanced neuromusculoskeletal model for simulating postural control of upright standing.

The human's upright standing is a complex control process that is not yet fully understood. Postural control models can provide insights into the body's internal control processes of balance behavior. Using physiologically plausible models can also help explaining pathophysiological motion behavior. In this paper, we introduce a neuromusculoskeletal postural control model using sensor feedback consisting of somatosensory, vestibular and visual information. The sagittal plane model was restricted to effectively six degrees of freedom and consisted of nine muscles per leg. Physiologically plausible neural delays were considered for balance control. We applied forward dynamic simulations and a single shooting approach to generate healthy reactive balance behavior during quiet and perturbed upright standing. Control parameters were optimized to minimize muscle effort. We showed that our model is capable of fulfilling the applied tasks successfully. We observed joint angles and ranges of motion in physiologically plausible ranges and comparable to experimental data. This model represents the starting point for subsequent simulations of pathophysiological postural control behavior.

Inactivity-induced phrenic motor facilitation requires PKCζ activity within phrenic motor neurons.

Prolonged inhibition of respiratory neural activity elicits a long-lasting increase in phrenic nerve amplitude once respiratory neural activity is restored. Such long-lasting facilitation represents a form of respiratory motor plasticity known as inactivity-induced phrenic motor facilitation (iPMF). Although facilitation also occurs in inspiratory intercostal nerve activity after diminished respiratory neural activity (iIMF), it is of shorter duration. Atypical PKC activity in the cervical spinal cord is necessary for iPMF and iIMF, but the site and specific isoform of the relevant atypical PKC are unknown. Here, we used RNA interference to test the hypothesis that the zeta atypical PKC isoform (PKCζ) within phrenic motor neurons is necessary for iPMF but PKCζ within intercostal motor neurons is unnecessary for transient iIMF. Intrapleural injections of siRNAs targeting PKCζ (siPKCζ) to knock down PKCζ mRNA within phrenic and intercostal motor neurons were made in rats. Control rats received a nontargeting siRNA (NTsi) or an active siRNA pool targeting a novel PKC isoform, PKCθ (siPKCθ), which is required for other forms of respiratory motor plasticity. Phrenic nerve burst amplitude and external intercostal (T2) electromyographic (EMG) activity were measured in anesthetized and mechanically ventilated rats exposed to 30 min of respiratory neural inactivity (i.e., neural apnea) created by modest hypocapnia (20 min) or a similar recording duration without neural apnea (time control). Phrenic burst amplitude was increased in rats treated with NTsi (68 ± 10% baseline) and siPKCθ (57 ± 8% baseline) 60 min after neural apnea vs. time control rats (-3 ± 3% baseline), demonstrating iPMF. In contrast, intrapleural siPKCζ virtually abolished iPMF (5 ± 4% baseline). iIMF was transient in all groups exposed to neural apnea; however, intrapleural siPKCζ attenuated iIMF 5 min after neural apnea (50 ± 21% baseline) vs. NTsi (97 ± 22% baseline) and siPKCθ (103 ± 20% baseline). Neural inactivity elevated the phrenic, but not intercostal, responses to hypercapnia, an effect that was blocked by siPKCζ. We conclude that PKCζ within phrenic motor neurons is necessary for long-lasting iPMF, whereas intercostal motor neuron PKCζ contributes to, but is not necessary for, transient iIMF.NEW & NOTEWORTHY We report important new findings concerning the mechanisms regulating a form of spinal neuroplasticity elicited by prolonged inhibition of respiratory neural activity, inactivity-induced phrenic motor facilitation (iPMF). We demonstrate that the atypical PKC isoform PKCζ within phrenic motor neurons is necessary for long-lasting iPMF, whereas intercostal motor neuron PKCζ contributes to, but is not necessary for, transient inspiratory intercostal facilitation. Our findings are novel and advance our understanding of mechanisms contributing to phrenic motor plasticity.

The relationship between SGLT2 and systemic blood pressure regulation.

The sodium-glucose cotransporter 2 (SGLT2) is a glucose transporter that is located within the proximal tubule of the kidney's nephrons. While it is typically associated with the kidney, it was later identified in various areas of the central nervous system, including areas modulating cardiorespiratory regulation like blood pressure. In the kidney, SGLT2 functions by reabsorbing glucose from the nephron's tubule into the bloodstream. SGLT2 inhibitors are medications that hinder the function of SGLT2, thus preventing the absorption of glucose and allowing for its excretion through the urine. While SGLT2 inhibitors are not the first-line choice, they are given in conjunction with other pharmaceutical interventions to manage hyperglycemia in individuals with diabetes mellitus. SGLT2 inhibitors also have a surprising secondary effect of decreasing blood pressure independent of blood glucose levels. The implication of SGLT2 inhibitors in lowering blood pressure and its presence in the central nervous system brings to question the role of SGLT2 in the brain. Here, we evaluate and review the function of SGLT2, SGLT2 inhibitors, their role in blood pressure control, the future of SGLT2 inhibitors as antihypertensive agents, and the possible mechanisms of SGLT2 blood pressure control in the central nervous system.

Mobile neuroimaging: What we have learned about the neural control of human walking, with an emphasis on EEG-based research.

Our understanding of the neural control of human walking has changed significantly over the last twenty years and mobile brain imaging methods have contributed substantially to current knowledge. High-density electroencephalography (EEG) has the advantages of being lightweight and mobile while providing temporal resolution of brain changes within a gait cycle. Advances in EEG hardware and processing methods have led to a proliferation of research on the neural control of locomotion in neurologically intact adults. We provide a narrative review of the advantages and disadvantages of different mobile brain imaging methods, then summarize findings from mobile EEG studies quantifying electrocortical activity during human walking. Contrary to historical views on the neural control of locomotion, recent studies highlight the widespread involvement of many areas, such as the anterior cingulate, posterior parietal, prefrontal, premotor, sensorimotor, supplementary motor, and occipital cortices, that show active fluctuations in electrical power during walking. The electrocortical activity changes with speed, stability, perturbations, and gait adaptation. We end with a discussion on the next steps in mobile EEG research.

Chemogenetic stimulation of phrenic motor output and diaphragm activity.

Impaired diaphragm activation contributes to morbidity and mortality in many neurodegenerative diseases and neurologic injuries. We conducted experiments to determine if expression of an excitatory DREADD (designer receptors exclusively activation by designer drugs) in the mid-cervical spinal cord would enable respiratory-related activation of phrenic motoneurons to increase diaphragm activation. Wild type (C57/bl6) and ChAT-Cre mice received bilateral intraspinal (C4) injections of an adeno-associated virus (AAV) encoding the hM3D(Gq) excitatory DREADD. In wild type mice, this produced non-specific DREADD expression throughout the mid-cervical ventral horn. In ChAT-Cre mice, a Cre-dependent viral construct was used to drive DREADD expression in C4 ventral horn motoneurons, targeting the phrenic motoneuron pool. Diaphragm EMG was recorded during spontaneous breathing at 6-8 weeks post-AAV delivery. The selective DREADD ligand JHU37160 (J60) caused a bilateral, sustained (>1 hr) increase in inspiratory EMG bursting in both groups; the relative increase was greater in ChAT-Cre mice. Additional experiments in a ChAT-Cre rat model were conducted to determine if spinal DREADD activation could increase inspiratory tidal volume (VT) during spontaneous breathing without anesthesia. Three to four months after intraspinal (C4) injection of AAV driving Cre-dependent hM3D(Gq) expression, intravenous J60 resulted in a sustained (>30 min) increase in VT assessed using whole-body plethysmography. Subsequently, direct nerve recordings confirmed that J60 evoked a >50% increase in inspiratory phrenic output. The data show that mid-cervical spinal DREADD expression targeting the phrenic motoneuron pool enables ligand-induced, sustained increases in the neural drive to the diaphragm. Further development of this technology may enable application to clinical conditions associated with impaired diaphragm activation and hypoventilation.

Inhibition and potentiation of the exercise pressor reflex by pharmacological modulation of TRPC6 in male rats.

We determined the role played by the transient receptor potential canonical 6 (TRPC6) channel in evoking the mechanical component of the exercise pressor reflex in male decerebrated Sprague-Dawley rats. TRPC6 channels were identified by quadruple-labelled (DiI, TRPC6, neurofilament-200 and peripherin) immunohistochemistry in dorsal root ganglion (DRG) cells innervating the triceps surae muscles (n = 12). The exercise pressor reflex was evoked by statically contracting the triceps surae muscles before and after injection of the TRPC6 antagonist BI-749327 (n = 11; 12 µg kg-1 ) or SAR7334 (n = 11; 7 µg kg-1 ) or the TRPC6 positive modulator C20 (n = 11; 18 µg kg-1 ). Similar experiments were conducted while the muscles were passively stretched (n = 8-12), a manoeuvre that isolated the mechanical component of the reflex. Blood pressure, tension, renal sympathetic nerve activity (RSNA) and blood flow were recorded. Of the DRG cells innervating the triceps surae muscles, 85% stained positive for the TRPC6 antigen, and 45% of those cells co-expressed neurofilament-200. Both TRPC6 antagonists decreased the reflex pressor responses to static contraction (-32 to -42%; P < 0.05) and to passive stretch (-35 to -52%; P < 0.05), whereas C20 increased these responses (55-65%; P < 0.05). In addition, BI-749327 decreased the peak and integrated RSNA responses to both static contraction (-39 to -43%; P < 0.05) and passive stretch (-56 to -62%; P < 0.05), whereas C20 increased the RSNA to passive stretch only. The onset latency of the decrease or increase in RSNA occurred within 2 s of the onset of the manoeuvres (P < 0.05). Collectively, our results show that TRPC6 plays a key role in evoking the mechanical component of the exercise pressor reflex. KEY POINTS: The exercise pressor reflex plays a key role in the sympathetic and haemodynamic responses to exercise. This reflex is composed of two components, namely the mechanoreflex and the metaboreflex. The receptors responsible for evoking the mechanoreflex are poorly documented. A good candidate for this function is the transient receptor potential canonical 6 (TRPC6) channel, which is activated by mechanical stimuli and expressed in dorsal root ganglia of rats. Using two TRPC6 antagonists and one positive modulator, we investigated the role played by TRPC6 in evoking the mechanoreflex in decerebrated rats. Blocking TRPC6 decreased the renal sympathetic and the pressor responses to both contraction and stretch, the latter being a manoeuvre that isolates the mechanoreflex. In contrast, the positive modulator increased the pressor reflex to contraction and stretch, in addition to the sympathetic response to stretch. Our results provide strong support for a role played by the TRPC6 channel in evoking the mechanoreflex.

System of Implantable Electrodes for Neural Signal Acquisition and Stimulation for Wirelessly Connected Forearm Prosthesis.

There is great interest in the development of prosthetic limbs capable of complex activities that are wirelessly connected to the patient's neural system. Although some progress has been achieved in this area, one of the main problems encountered is the selective acquisition of nerve impulses and the closing of the automation loop through the selective stimulation of the sensitive branches of the patient. Large-scale research and development have achieved so-called "cuff electrodes"; however, they present a big disadvantage: they are not selective. In this article, we present the progress made in the development of an implantable system of plug neural microelectrodes that relate to the biological nerve tissue and can be used for the selective acquisition of neuronal signals and for the stimulation of specific nerve fascicles. The developed plug electrodes are also advantageous due to their small thickness, as they do not trigger nerve inflammation. In addition, the results of the conducted tests on a sous scrofa subject are presented.

Reliability and minimal detectable change of stiffness and other mechanical properties of the ankle joint in standing and walking.

BACKGROUND: Ankle joint stiffness and viscosity are fundamental mechanical descriptions that govern the movement of the body and impact an individual's walking ability. Hence, these internal properties of a joint have been increasingly used to evaluate the effects of pathology (e.g., stroke) and in the design and control of robotic and prosthetic devices. However, the reliability of these measurements is currently unclear, which is important for translation to clinical use. RESEARCH QUESTION: Can we reliably measure the mechanical impedance parameters of the ankle while standing and walking? METHODS: Eighteen able-bodied individuals volunteered to be tested on two different days separated by at least 24 h. Participants received several small random ankle dorsiflexion perturbations while standing and during the stance phase of walking using a custom-designed robotic platform. Three-dimensional motion capture cameras and a 6-component force plate were used to quantify ankle joint motions and torque responses during normal and perturbed conditions. Ankle mechanical impedance was quantified by computing participant-specific ensemble averages of changes in ankle angle and torque due to perturbation and fitting a second-order parametric model consisting of stiffness, viscosity, and inertia. The test-retest reliability of each parameter was assessed using intraclass correlation coefficients (ICCs). We also computed the minimal detectable change (MDC) for each impedance parameter to establish the smallest amount of change that falls outside the measurement error of the instrument. RESULTS: In standing, the reliability of stiffness, viscosity, and inertia was good to excellent (ICCs=0.67-0.91). During walking, the reliability of stiffness and viscosity was good to excellent (ICCs=0.74-0.84) while that of inertia was fair to good (ICCs=0.47-0.68). The MDC for a single subject ranged from 20%- 65% of the measurement mean but was higher (>100%) for inertia during walking. SIGNIFICANCE: Results indicate that dynamic measures of ankle joint impedance were generally reliable and could serve as an adjunct clinical tool for evaluating gait impairments.

Dynamic learning from adaptive neural control for full-state constrained strict-feedback nonlinear systems.

This study focuses on the learning and control issues of strict-feedback systems with full-state constraints. To achieve learning capability under constraints, transformation mapping is utilized to convert the original system with full-state constraints into a quasi-pure-feedback unconstrained system. Utilizing the system transformation technique, only a single neural network (NN) is required to identify the unknown dynamics within the transformed system. Combining the dynamic surface control design, a novel adaptive neural control scheme is developed to ensure that all closed-loop signals are uniformly bounded, and every system state remains within the predefined constraint range. In addition, the precise convergence of NN weights is further transformed into an exponential stability problem for a category of linear time-varying systems under persistent excitation conditions. Subsequently, the converged NN weights are efficiently stored and utilized to create a learning controller to achieve better control performance while abiding by the full-state constraints. The viability of this control strategy is demonstrated via simulations.

Predictive simulations identify potential neuromuscular contributors to idiopathic toe walking.

BACKGROUND: Most cases of toe walking in children are idiopathic. We used pathology-specific neuromusculoskeletal predictive simulations to identify potential underlying neural and muscular mechanisms contributing to idiopathic toe walking. METHODS: A musculotendon contracture was added to the ankle plantarflexors of a generic musculoskeletal model to represent a pathology-specific contracture model, matching the reduced ankle dorsiflexion range-of-motion in a cohort of children with idiopathic toe walking. This model was employed in a forward dynamic simulation controlled by reflexes and supraspinal drive, governed by a multi-objective cost function to predict gait patterns with the contracture model. We validated the predicted gait using experimental gait data from children with idiopathic toe walking with ankle contracture, by calculating the root mean square errors averaged over all biomechanical variables. FINDINGS: A predictive simulation with the pathology-specific model with contracture approached experimental ITW data (root mean square error = 1.37SD). Gastrocnemius activation was doubled from typical gait simulations, but lacked a peak in early stance as present in electromyography. This synthesised idiopathic toe walking was more costly for all cost function criteria than typical gait simulation. Also, it employed a different neural control strategy, with increased length- and velocity-based reflex gains to the plantarflexors in early stance and swing than typical gait simulations. INTERPRETATION: The simulations provide insights into how a musculotendon contracture combined with altered neural control could contribute to idiopathic toe walking. Insights into these neuromuscular mechanisms could guide future computational and experimental studies to gain improved insight into the cause of idiopathic toe walking.

Simultaneous Sensing and Actuating Capabilities of a Triple-Layer Biomimetic Muscle for Soft Robotics.

This work presents the fabrication and characterization of a triple-layered biomimetic muscle constituted by polypyrrole (PPy)-dodecylbenzenesulfonate (DBS)/adhesive tape/PPy-DBS demonstrating simultaneous sensing and actuation capabilities. The muscle was controlled by a neurobiologically inspired cortical neural network sending agonist and antagonist signals to the conducting polymeric layers. Experiments consisted of controlled voluntary movements of the free end of the muscle at angles of ±20°, ±30°, and ±40° while monitoring the muscle's potential response. Results show the muscle's potential varies linearly with applied current amplitude during actuation, enabling current sensing. A linear dependence between muscle potential and temperature enabled temperature sensing. Electrolyte concentration changes also induced exponential variations in the muscle's potential, allowing for concentration sensing. Additionally, the influence of the electric current density on the angular velocity, the electric charge density, and the desired angle was studied. Overall, the conducting polymer-based soft biomimetic muscle replicates properties of natural muscles, permitting simultaneous motion control, current, temperature, and concentration sensing. The integrated neural control system exhibits key features of biological motion regulation. This muscle actuator with its integrated sensing and control represents an advance for soft robotics, prosthetics, and biomedical devices requiring biomimetic multifunctionality.

Adaptive Autonomic and Neuroplastic Control in Diabetic Neuropathy: A Narrative Review.

BACKGROUND: Type 2 diabetes mellitus (T2DM) is a worldwide socioeconomic burden, and is accompanied by a variety of metabolic disorders, as well as nerve dysfunction referred to as diabetic neuropathy (DN). Despite a tremendous body of research, the pathogenesis of DN remains largely elusive. Currently, two schools of thought exist regarding the pathogenesis of diabetic neuropathy: a) mitochondrial-induced toxicity, and b) microvascular damage. Both mechanisms signify DN as an intractable disease and, as a consequence, therapeutic approaches treat symptoms with limited efficacy and risk of side effects. OBJECTIVE: Here, we propose that the human body exclusively employs mechanisms of adaptation to protect itself during an adverse event. For this purpose, two control systems are defined, namely the autonomic and the neural control systems. The autonomic control system responds via inflammatory and immune responses, while the neural control system regulates neural signaling, via plastic adaptation. Both systems are proposed to regulate a network of temporal and causative connections which unravel the complex nature of diabetic complications. RESULTS: A significant result of this approach infers that both systems make DN reversible, thus opening the door to novel therapeutic applications.

Functional knockout of the TRPV1 channel has no effect on the exercise pressor reflex in rats.

The role played by the transient receptor potential vanilloid 1 (TRPV1) channel on the thin fibre afferents evoking the exercise pressor reflex is controversial. To shed light on this controversy, we compared the exercise pressor reflex between newly developed TRPV1+/+ , TRPV1+/- and TRPV1-/- rats. Carotid arterial injection of capsaicin (0.5 µg), evoked significant pressor responses in TRPV1+/+ and TRPV1+/- rats, but not in TRPV1-/- rats. In acutely isolated dorsal root ganglion neurons innervating the gastrocnemius muscles, capsaicin evoked inward currents in neurons isolated from TRPV1+/+ and TRPV1+/- rats but not in neurons isolated from TRPV1-/- rats. The reflex was evoked by stimulating the tibial nerve in decerebrated rats whose femoral artery was either freely perfused or occluded. We found no difference between the reflex in the three groups of rats regardless of the patency of the femoral artery. For example, the peak pressor responses to contraction in TRPV1+/+ , TRPV1+/- and TRPV1-/- rats with patent femoral arteries averaged 17.1 ± 7.2, 18.9 ± 12.4 and 18.4 ± 8.6 mmHg, respectively. Stimulation of the tibial nerve after paralysis with pancuronium had no effect on arterial pressure, findings which indicated that the pressor responses to contraction were not caused by electrical stimulation of afferent tibial nerve axons. We also found that expression levels of acid-sensing ion channel 1 and endoperoxide 4 receptor in the L4 and 5 dorsal root ganglia were not upregulated in the TRPV1-/- rats. We conclude that TRPV1 is not needed to evoke the exercise pressor reflex in rats whose contracting muscles have either a patent or an occluded arterial blood supply. KEY POINTS: A reflex arising in contracting skeletal muscle contributes to the increases in arterial blood pressure, cardiac output and breathing evoked by exercise. The sensory arm of the reflex comprises both mechanoreceptors and metaboreceptors, of which the latter signals that blood flow to exercising muscle is not meeting its metabolic demand. The nature of the channel on the metaboreceptor sensing a mismatch between supply and demand is controversial; some believe that it is the transient receptor potential vanilloid 1 (TRPV1) channel. Using genetically engineered rats in which the TRPV1 channel is rendered non-functional, we have shown that it is not needed to evoke the metaboreflex.

Using neurons to maintain autonomy: Learning from C. elegans.

Understanding how biological organisms are autonomous-maintain themselves far from equilibrium through their own activities-requires understanding how they regulate those activities. In multicellular animals, such control can be exercised either via endocrine signaling through the vasculature or via neurons. In C. elegans this control is exercised by a well-delineated relatively small but distributed nervous system that relies on both chemical and electric transmission of signals. This system provides resources to integrate information from multiple sources as needed to maintain the organism. Especially important for the exercise of neural control are neuromodulators, which we present as setting agendas for control through more traditional electrical signaling. To illustrate how the C. elegans nervous system integrates multiple sources of information in controlling activities important for autonomy, we focus on feeding behavior and responses to adverse conditions. We conclude by considering how a distributed nervous system without a centralized controller is nonetheless adequate for autonomy.

Hybrid learning mechanisms under a neural control network for various walking speed generation of a quadruped robot.

Legged robots that can instantly change motor patterns at different walking speeds are useful and can accomplish various tasks efficiently. However, state-of-the-art control methods either are difficult to develop or require long training times. In this study, we present a comprehensible neural control framework to integrate probability-based black-box optimization (PIBB) and supervised learning for robot motor pattern generation at various walking speeds. The control framework structure is based on a combination of a central pattern generator (CPG), a radial basis function (RBF) -based premotor network and a hypernetwork, resulting in a so-called neural CPG-RBF-hyper control network. First, the CPG-driven RBF network, acting as a complex motor pattern generator, was trained to learn policies (multiple motor patterns) for different speeds using PIBB. We also introduce an incremental learning strategy to avoid local optima. Second, the hypernetwork, which acts as a task/behavior to control parameter mapping, was trained using supervised learning. It creates a mapping between the internal CPG frequency (reflecting the walking speed) and motor behavior. This map represents the prior knowledge of the robot, which contains the optimal motor joint patterns at various CPG frequencies. Finally, when a user-defined robot walking frequency or speed is provided, the hypernetwork generates the corresponding policy for the CPG-RBF network. The result is a versatile locomotion controller which enables a quadruped robot to perform stable and robust walking at different speeds without sensory feedback. The policy of the controller was trained in the simulation (less than 1 h) and capable of transferring to a real robot. The generalization ability of the controller was demonstrated by testing the CPG frequencies that were not encountered during training.

Ankle Strategies for Step-Aside Movement during Straight Walking.

The step-aside movement, also known as the dodging step, is a common maneuver for avoiding obstacles while walking. However, differences in neural control mechanisms and ankle strategies compared to straight walking can pose a risk of falling. This study aimed to examine the differences in tibialis anterior (TA), peroneus longus (PL), and soleus (SOL) muscle contractions, foot center of pressure (CoP) displacement, and ground reaction force (GRF) generation between step-aside movement and straight walking to understand the mechanism behind step-aside movement during walking. Twenty healthy young male participants performed straight walking and step-aside movements at comfortable walking speeds. The participants' muscle contractions, CoP displacement, and GRF were measured. The results show significant greater bilateral ankle muscle contractions during the push and loading phases of step-aside movement than during straight walking. Moreover, the CoP displacement, GRF generation mechanism, and timing differed from those observed during straight walking. These findings provide valuable insights for rehabilitation professionals in the development of clinical decisions for populations at a risk of falls and lacking gait stability.